p16/cyclin-dependent kinase inhibitor 2A deficiency in human melanocyte senescence, apoptosis, and immortalization: possible implications for melanoma progression. (Q40646165)

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scientific article published on May 2003

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English	p16/cyclin-dependent kinase inhibitor 2A deficiency in human melanocyte senescence, apoptosis, and immortalization: possible implications for melanoma progression.	scientific article published on May 2003

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3 November 2019

p16/cyclin-dependent kinase inhibitor 2A deficiency in human melanocyte senescence, apoptosis, and immortalization: possible implications for melanoma progression (English)

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3 November 2019

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3 November 2019

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Elena V Sviderskaya

1

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3 November 2019

Vanessa C Gray-Schopfer

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3 November 2019

Simon P Hill

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3 November 2019

Tracy J Evans-Whipp

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3 November 2019

Jane Bond

6

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Lucy Hill

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Veronique Bataille

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3 November 2019

Gordon Peters

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David Kipling

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3 November 2019

David Wynford-Thomas

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3 November 2019

Dorothy C Bennett

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1 May 2003

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3 November 2019

Journal of the National Cancer Institute

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723-732

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3 November 2019

The INK4A/ARF locus and its two gene products

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p16(MTS-1/CDKN2/INK4a) in cancer progression

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The INK4a/ARF network in tumour suppression

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Alternative reading frames of the INK4a tumor suppressor gene encode two unrelated proteins capable of inducing cell cycle arrest

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A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4

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The alternative product from the human CDKN2A locus, p14(ARF), participates in a regulatory feedback loop with p53 and MDM2.

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Tumor suppression at the mouse INK4a locus mediated by the alternative reading frame product p19ARF

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The Ink4a tumor suppressor gene product, p19Arf, interacts with MDM2 and neutralizes MDM2's inhibition of p53

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ARF promotes MDM2 degradation and stabilizes p53: ARF-INK4a locus deletion impairs both the Rb and p53 tumor suppression pathways

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Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis

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Loss of p16Ink4a confers susceptibility to metastatic melanoma in mice

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Expression of the p16INK4a tumor suppressor versus other INK4 family members during mouse development and aging.

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The age of cancer

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Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a

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Identification of human tumour suppressor genes by monochromosome transfer: rapid growth-arrest response mapped to 9p21 is mediated solely by the cyclin-D-dependent kinase inhibitor gene, CDKN2A (p16INK4A).

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Role of p14(ARF) in replicative and induced senescence of human fibroblasts

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Role of the INK4a locus in tumor suppression and cell mortality.

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Terminal differentiation and senescence in the human melanocyte: repression of tyrosine-phosphorylation of the extracellular signal-regulated kinase 2 selectively defines the two phenotypes

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Molecular regulation of melanocyte senescence

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Biallelic mutations in p16(INK4a) confer resistance to Ras- and Ets-induced senescence in human diploid fibroblasts

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Homozygous germline mutation of CDKN2A/p16 and glucose-6-phosphate dehydrogenase deficiency in a multiple melanoma case

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Both Rb/p16INK4a inactivation and telomerase activity are required to immortalize human epithelial cells.

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Putative telomere-independent mechanisms of replicative aging reflect inadequate growth conditions

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Complementation of hypopigmentation in p-mutant (pink-eyed dilution) mouse melanocytes by normal human P cDNA, and defective complementation by OCA2 mutant sequences

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Involvement of the cyclin-dependent kinase inhibitor p16 (INK4a) in replicative senescence of normal human fibroblasts

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